RESUMO
Fibromyalgia may present with widespread pain and tenderness, fatigue, anxiety, and depression and is associated with a low pain threshold. The etiology of fibromyalgia is yet to be ascertained, although both genetic and environmental factors may play a role in the susceptibility of patients to fibromyalgia. Various genetic variations have been investigated to explain fibromyalgia susceptibility and differences in pain sensitivity, pain threshold, and tolerance. The A118G rs1799971 polymorphism in the opioid receptor µ1 gene (OPRM1) is one of the candidate genes. We hypothesized that the OPRM1 polymorphism may play a role in fibromyalgia susceptibility and impact the pain intensity and pain-related symptoms in fibromyalgia patients. This study comprised of 108 patients with fibromyalgia and 100 healthy controls. Overall, the 118G allele frequency was 16.3 % and was significantly lower in patients with fibromyalgia than in the control group (13.9 and 19 %, respectively). No difference was observed between fibromyalgia patients with and without the A118G allele with regard to the Beck Depression Inventory, widespread pain index, symptom severity, and Fibromyalgia Impact Questionnaire scores. All body parts of patients with fibromyalgia demonstrated lower pressure pain thresholds (PPT) compared to controls. The PPTs were higher in the 118 A/A genotype carrier fibromyalgia patients than in 118*/G carriers; however, the differences were not significant. As the A118G polymorphism frequency was lower in fibromyalgia patients, this polymorphism may exert a protective effect against fibromyalgia in Turkish women. However, the OPRM1 polymorphism does not have a significant effect on pressure pain and fibromyalgia severity.
Assuntos
Fibromialgia/genética , Dor/genética , Polimorfismo Genético , Receptores Opioides mu/genética , Adulto , Estudos de Casos e Controles , Feminino , Fibromialgia/diagnóstico , Fibromialgia/epidemiologia , Fibromialgia/fisiopatologia , Frequência do Gene , Estudos de Associação Genética , Predisposição Genética para Doença , Humanos , Dor/diagnóstico , Dor/epidemiologia , Dor/fisiopatologia , Medição da Dor , Limiar da Dor , Fenótipo , Valor Preditivo dos Testes , Fatores de Proteção , Fatores de Risco , Índice de Gravidade de Doença , Fatores Sexuais , Turquia/epidemiologiaRESUMO
The present study was undertaken to evaluate genotoxic potential of two auxinic herbicides [2,4-dicholorophenoxy acetic acid (2,4-D) and 3,6-dichloro-2-methoxybenzoic acid (Dicamba)] in the roots of common bean (Phaseolus vulgaris L.) seedlings. Two-day-old etiolated seedlings were treated with 10 ppm methyl methanesulfonate (MMS, positive control) or 0.1, 0.2, or 0.3 ppm of either 2,4-D or Dicamba. At the end of a 96 h growth period, root growth, total soluble protein content, DNA damage in individual cells (comet assay scores) and randomly amplified polymorphic DNA (RAPD) profiles were used as endpoints of genotoxicity. 2,4-D and Dicamba were clearly dose-dependent root growth inhibitors. Total soluble protein content was significantly decreased in the positive control and at high concentrations (0.2 and 0.3 ppm) of Dicamba. Soluble protein content increased significantly only at 0.3 ppm 2,4-D (P<0.05). In the comet assay, DNA fragmentation increased in a dose-dependent manner. The diagnostic and phenetic analyzes of appeared and/or disappeared RAPD bands indicated that dose-dependent DNA polymorphism was induced by both herbicides. Genomic template stability was significantly affected at all 2,4-D and Dicamba doses tested. Overall 2,4-D and Dicamba have similar effects on DNA damage detected by comet and RAPD assays.
Assuntos
Ácido 2,4-Diclorofenoxiacético/toxicidade , Fragmentação do DNA/efeitos dos fármacos , Dicamba/toxicidade , Herbicidas/toxicidade , Phaseolus/efeitos dos fármacos , Plântula/efeitos dos fármacos , Análise de Variância , Ensaio Cometa , Primers do DNA/genética , Relação Dose-Resposta a Droga , Raízes de Plantas/efeitos dos fármacos , Raízes de Plantas/crescimento & desenvolvimento , Técnica de Amplificação ao Acaso de DNA PolimórficoRESUMO
Apolipoprotein E (ApoE) gene polymorphisms are thought to be the most important genetic risk factor in the pathogenesis of late onset and sporadic Alzheimer's disease (AD). Moreover, interleukin-1α (IL-1α) is found to be associated with the pathogenesis of AD. In this research, ∊2, ∊3, and ∊4 polymorphisms of ApoE gene and C889T polymorphism of IL-1α gene were genotyped in patients with AD and controls. Genotyping was performed by real-time polymerase chain reaction. ∊3/∊3 and ∊3/∊4 genotype frequencies were significantly higher in control and case groups, respectively. While ∊3 allele frequencies were significantly higher in the control group, ∊2 and ∊4 allele frequencies were significantly higher among the cases with AD. No difference was found between the groups according to C889T polymorphism of IL-1α. In conclusion, we demonstrated that there was a strong association between ApoE ∊4 allele and AD, while there was no relation with IL-1α C889T polymorphisms for this study.